Some cells can turn cancerous when they divide, due to chromosomes getting “lost” in the process. In a new study, researchers at the University of Warwick have uncovered what happens to these lost chromosomes and how to recover them, potentially leading to new treatments to prevent certain cancers.
Before a cell divides, it first duplicates all of its chromosomes, then gives a copy to each of the two new cells. This is done using a protein structure called a mitotic spindle, which pulls chromosomes towards each end of the mother cell before it divides.
However it’s not always a clean process. Sometimes the daughter cells will end up with the wrong numbers of chromosomes, and these faults can affect their function and future division. When this happens, the cells are described as aneuploid. This applies to many cancer cells, including more than two-thirds of solid tumors.
Investigating how and why this happens could lead to new ways to prevent some forms of cancer. And now, the Warwick researchers say they’ve uncovered new details on that process. They found that chromosomes can become tangled in the densely-packed membranes around the spindle, preventing them from being sorted into the daughter cells.
When the researchers used a technique called organelle relocalization to untangle those membranes, the spindle was once again able to grab the chromosomes, and the cell division became healthy again. This, they say, shows that chromosomes lost in this way can be a direct risk factor for cancerous cells.
“Many scientists working on cell division focus on the spindle: how it works and why it makes mistakes in cancer,” said Stephen Royle, corresponding author of the study. “In this paper we shifted the spotlight and looked at membranes inside dividing cells.”
The team says that finding a way to fix the tangles that entrap chromosomes could help prevent some forms of cancer. However, at this early stage the research is mostly about understanding the process, and much more work needs to be done to find a way to perform this fix in cells in vivo.
The research was published in the Journal of Cell Biology.
Source: University of Warwick